Type 2 diabetes is characterized by pancreatic beta-cell dysfunction and insulin resistance, and the number of patients has markedly increased worldwide. In the diabetic state, hyperglycemia per se and subsequent induction of oxidative stress decrease insulin biosynthesis and secretion, leading to the aggravation of Type 2 diabetes. In addition, there is substantial reduction in expression and/or activities of several insulin gene transcription factors. This process is known as beta-cell glucose toxicity, which is often observed under diabetic conditions. Taken together, it is likely that oxidative stress explains, at least in part, the molecular mechanism for beta-cell glucose toxicity, which is often observed in Type 2 diabetes.